ArticleClinical and experimental medicine2020
B7-H4 facilitates proliferation and metastasis of colorectal carcinoma cell through PI3K/Akt/mTOR signaling pathway.
Article in Clinical and experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 33 citations in OpenAlex.
- Membrane and soluble VTCN1 (B7H4) converge on Src signaling to mediate gemcitabine resistance in intrahepatic cholangiocarcinoma.Theranostics · 2026Article
- Immune checkpoint blockade for cancer therapy: current progress and perspectives.Journal of Zhejiang University. Science. B · 2025Review
- B7H4 Role in Solid Cancers: A Review of the Literature.Cancers · 2024Review
- Depletion of B7-H4 from C3H10 T1/2 Mesenchymal Stem Cells Attenuates their Immunomodulatory Therapy in Experimental Autoimmune Encephalomyelitis Mice.Neurotoxicity research · 2022Article
- B7-H4 expression is upregulated by PKCδ activation and contributes to PKCδ-induced cell motility in colorectal cancer.Cancer cell international · 2022Article
- B7 family member H4 induces epithelial-mesenchymal transition and promotes the proliferation, migration and invasion of colorectal cancer cells.Bioengineered · 2022Article
- The expression pattern of Immune checkpoints after chemo/radiotherapy in the tumor microenvironment.Frontiers in immunology · 2022Review
- Clinical Research on the Mechanisms Underlying Immune Checkpoints and Tumor Metastasis.Frontiers in oncology · 2021Review
- Nobiletin alleviates ischemia/reperfusion injury in the kidney by activating PI3K/AKT pathway.Molecular medicine reports · 2020Article
- Hydrogen Sulfide-Evoked Intracellular CaCancers · 2020Article
- B7-H3 immune checkpoint expression is a poor prognostic factor in colorectal carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Overexpression of B7-H4 promotes renal cell carcinoma progression by recruiting tumor-associated neutrophils via upregulation of CXCL8.Oncology letters · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B7-H4 is over-expressed in various tumors and may affect many aspects of cancer biology. Our previous studies have reported that the over-expressed B7-H4 in serum or tumor tissue of colorectal carcinoma (CRC) patients was closely related to CRC progression. However, B7-H4 in cell biological characteristics of CRC is not well studied. Here, we investigate the effect of the B7-H4 on cell proliferation, migration and its expression regulated by PI3K/Akt/mTOR signaling pathway in CRC. Firstly, pSilencer 4.1-B7-H4-shRNA vector was constructed and stable transfection was performed on HT-29 cells. Secondly, cell proliferation, cell cycle, cell apoptosis and cell migration were evaluated after B7-H4 silencing, and the expression of Bcl-2, caspase-3, MMP-2 and MMP-9 was also measured. Finally, the regulation of B7-H4 by PI3K/Akt/mTOR signaling pathway was measured followed by treatment with or without PI3K/Akt and mTOR inhibitor. The results showed that the viability of HT-29 cells was significantly decreased after B7-H4 silencing (P < 0.05). B7-H4 silencing significantly increased the apoptosis rate and caspase-3 protein expression while decreased Bcl-2 protein expression (P all < 0.05). B7-H4 silencing also significantly reduced the migration of HT-29 cells (P < 0.01) and the secretion of MMP-2 or MMP-9 (P all < 0.05). Following treatment with PI3K/Akt and mTOR inhibitor in HT-29 cells, the expression of B7-H4 was significantly downregulated compared with untreated group (P all < 0.05). Our results strongly suggest that B7-H4 may be involved in cell proliferation and migration by PI3K/Akt/mTOR signaling pathway. Therefore, blocking B7-H4 signaling might be a novel treatment strategy for CRC.
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